The broad purpose of this work is to further understand how microorganisms and vaccine adjuvants via their interaction with antigen presenting cells, such as macrophages and dendritic cells, affect the generation of T cell mediated immune responses via their ability to regulate the production of critical cytokines, such as IL-12 and IL-10. We have focused our work on the regulation of IL-12 production by G-protein signaling. Over the past year we have demonstrated that signaling via the chemoattractant receptor for formyl-peptides (such as f-met-leu-phe), the formyl-peptide receptor (FPR) significantly inhibits IL-12 production from human monocytes. We extended this finding to demonstrate that a peptide from HIV gp41, called T-20, which can bind to FPR can similarly suppress IL-12 production. the production of other cytokines, such as IL-10, and TNF-alpha were not affected. This data is important since it shows a pathway by which HIV could use to suppress the induction of protective Th-1 T cell responses that are dependent on IL-12 for their generation and maintanence. It also demonstrates for the first time that FPR is a promiscous receptor that has may effect both innate and adaptive immunity.